In 1990, Carthew and Robin (1) characterized a Drosophila gene which they named Seven IN Absentia (SINA). This gene was shown to be required for photoreceptor cell formation during Drosophila eye development. The SINA gene product was localized to the nuclei, where it was believed to act by regulating gene expression during cell differentiation within the Ras/Raf signal transduction pathway (1). Several vertebrate SINA homologues (Siah) have also been isolated and characterized. For example, Della et al. (2) reported identification of a Siah gene family in mice which fall in two groups termed SIAH-1 and SIAH-2. Based on the developmental expression patterns and high degree of homology between SIAH and SINA, a significant role in vertebrate development was proposed (2). Human homologues of SINA (HuSIAH-1 and HuSIAH-2) characterized by Hu et al. (3) were also found to be highly identical to the Drosophila proteins. A 282 amino acid protein is encoded by mammalian SIAH-1 whereas SIAH-2 encodes a 324 amino acid protein. All homologues reported so far contain a signature RING finger domain (1-3). Recent studies have suggested that the mammalian SINA homologues may be induced during programmed cell death or apoptosis (4, 5) and the ubiquitin-mediated protein degradation pathway (6). An Arabidopsis genomic sequence encoding a 305 amino acid protein with homology to SINA (Accession No. P93748) and a partial coding sequence for a Zea mays SINA homolog (Accession No. AF061511) have been deposited in Genbank.
The need to modulate plant cell development and apoptosis for such applications as the creation of male sterile plants is clear. Further, what is needed in the art is the means to control DNA repair/recombination pathways to modulate the efficiency with which heterologous nucleic acids are incorporated into the genomes of a target plant cell. Control of these processes has important implications in the creation of novel recombinantly engineered crops such as maize. The present invention provides these and other advantages.